Citation

Abstract

The accumulation of oligomeric species of
b-amyloid protein in the brain is considered to be a key
factor that causes Alzheimer’s disease (AD). However,
despite many years of research, the mechanism of neurotoxicity
in AD remains obscure. Recent evidence strongly
supports the theory that Ca2+ dysregulation is involved in
AD. Amyloid proteins have been found to induce Ca2+
influx into neurons, and studies on transgenic mice suggest
that this Ca2+ influx may alter neuronal excitability. The
identification of a risk factor gene for AD that may be
involved in the regulation of Ca2+ homeostasis and recent
findings which suggest that presenilins may be involved in
the regulation of intracellular Ca2+ stores provide converging
lines of evidence that support the idea that Ca2+
dysregulation is a key step in the pathogenesis of AD.